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Asthma
Pathophysiology Asthma is a chronic inflammatory disease of the airways that effects 7 million children in the United States. Exacerbating factors in pediatric patients tend to be external stimuli, such as pollen and dander. The physiological response to these antigens is very similar to the respiratory effects of anaphylaxis. An IgE -> Mast Cell -> Histamine response is initiated, but because the antigens are not in the bloodstream the symptoms are almost exclusively seen in the respiratory tract. Release of histamine in the bronchial wall results in the following: Vasodilation with edema Smooth muscle contraction (bronchoconstriction) Increased mucus secretion The combination of constricting airways and increased mucus production leads to mucus plugging of the bronchioles and higher resistance to airflow. The alveoli are being hypoventilated at this point and a ventilation-perfusion mismatch occurs. The resulting carbon dioxide retention and hypoxemia lead to hyperventilation and further air trapping. As this cycle continues, the muscles of respiration continue to fatigue and the problem only grows. In a severe, prolonged asthma attack, pressure will build in the thoracic cavity, limiting the venous return to the right side of the heart and dropping cardiac output. Syncope and hypotension are possible. The leading causes of death in an asthma attack are as follows: Severe bronchospasm and mucus plugging leading to asphyxia Dysrhythmias caused by hypoxia Tension Pneumothorax (generally bilateral)3 Clinical Presentation General appearance of the patient will be dyspnea, cough, and wheezing with prolonged expiration. They will not likely be able to speak more than a few words at a time. A late sign of sever asthma is a "silent chest", indicating that no air is able to be moved through the bronchial tree. Monitoring mental status is important in moderate to severe asthma attacks, as fatigue and decreased level of consciousness are two signs of a deteriorating patient. Relative tachycardia and tachypnea, a low SpO2 sat, and EtCO2 > 45mmHg are all signs of a severe episode.2 Prehospital Management Providers must be extremely aggressive in managing a severe pediatric asthma attack. Ask about the patient's PMHx. Have they had bad attacks before? What happened then? Have they ever been intubated?(2) Therapy begins with carefully assessing the potency of the airway, auscultating breath sounds, and administering high flow O2. The main treatment for asthma is albuterol, with the option of adding Ipratropium. 2.5-5.0 mg Albuterol +/- 0.5 mg Ipratropium via nebulizer, prn Corticosteroids are added as well. Methylprednisolone (Solu Medrol) is administered at 2 mg/kg IV bolus. If O2, a B2 agonist, and Solu Medrol have failed to stabilize the patient, the following therapies are indicated: 1:1000 Epi 0.01 mg/kg IM, max 0.5 mg ***Note: Epi has a short half-life and will only serve as a temporary stopgap, not a solution*** 6 Magnesium Sulfate 25-75 mg/kg IV infusion over 10 minutes Terbutaline 0.1 mg/kg, max 0.4 mg, q 15 min x3 **At this point in treatment, if the patient is still deteriorating, intubation and the care of a dedicated PICU or ICU are indicated.1,6 References 1) Engorn B, Flerlage J, eds. The Harriet Lane Handbook, 20th ed. Philadelphia, PA: Elsevier Saunders; 2015. 2) Sanders MJ. Mosby’s Paramedic Textbook. Burlington, MA: Jones & Bartlett Learning; 2012. 3) Hammer GD, McPhee SJ, eds. Pathophysiology of Disease - An Introduction to Clinical Medicine, 7th ed. New York, NY: McGraw-Hill Education; 2014. 4) Broaddus VC. Murray and Nadel’s Textbook of Respiratory Medicine. Philadelphia, PA: Elsevier Saunders; 2016. 5) Cline DM, Ma OJ. Tintinalli’s Emergency Medicine: Just the Facts, 3rd ed. New York, NY: The McGraw-Hill Companies, Inc.; 2013. 6) Caroline NL, Elling B, Smith M. Nancy Caroline’s Emergency Care in the Streets, 7th ed. Burlington, MA: Jones & Bartlett Learning; 2012